Role of renal nerves in compensatory adaptation to chronic reductions in sodium intake

Mizelle, H. L.; Hall, J. E.; Woods, L. L.; Montani, Jean‐Pierre; Dzielak, David J.; Pan, Yi

doi:10.1152/ajprenal.1987.252.2.f291

Cited by 20 publications

(35 citation statements)

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“…However, as the deviation in sodium balance was transient, this is unlikely to explain the chronic decrease in MABP. In the absence of lasting changes in sodium balance (compared to the steady positive balance of appropriate control animals), the present 20% decrease in PRC, confirming previous results of renal denervation (8,18), does not provide a convincing explanation of the relative hypotension. Only further studies, including measurements of sympathetic tone and vasoactive hormones, may disclose these mechanisms.…”

Section: Discussionsupporting

confidence: 66%

Renal nerves and nNOS: roles in natriuresis of acute isovolumetric sodium loading in conscious rats

Kompanowska-Jezierska

Wolff²,

Kuczeriszka³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Kompanowska-Jezierska E, Wolff H, Kuczeriszka M, Gramsbergen JB, Walkowska A, Johns EJ, Bie P. Renal nerves and nNOS: roles in natriuresis of acute isovolumetric sodium loading in conscious rats. Am J Physiol Regul Integr Comp Physiol 294: R1130-R1139, 2008. First published January 30, 2008 doi:10.1152/ajpregu.00908.2007.-It was hypothesized that renal sympathetic nerve activity (RSNA) and neuronal nitric oxide synthase (nNOS) are involved in the acute inhibition of renin secretion and the natriuresis following slow NaCl loading (NaLoad) and that RSNA participates in the regulation of arterial blood pressure (MABP). This was tested by NaLoad after chronic renal denervation with and without inhibition of nNOS by S-methyl-thiocitrulline (SMTC). In addition, the acute effects of renal denervation on MABP and sodium balance were assessed. Rats were investigated in the conscious, catheterized state, in metabolic cages, and acutely during anesthesia. NaLoad was performed over 2 h by intravenous infusion of hypertonic solution (50 mol ⅐ min Ϫ1 ⅐ kg body mass Ϫ1 ) at constant body volume conditions. SMTC was coinfused in amounts (20 g ⅐ min Ϫ1 ⅐ kg Ϫ1 ) reported to selectively inhibit nNOS. Directly measured MABPs of acutely and chronically denervated rats were less than control (15% and 9%, respectively, P Ͻ 0.005). Plasma renin concentration (PRC) was reduced by renal denervation (14.5 Ϯ 0.2 vs. 19.3 Ϯ 1.3 mIU/l, P Ͻ 0.005) and by nNOS inhibition (12.4 Ϯ 2.3 vs. 19.6 Ϯ 1.6 mlU/l, P Ͻ 0.005). NaLoad reduced PRC (P Ͻ 0.05) and elevated MABP modestly (P Ͻ 0.05) and increased sodium excretion six-fold, irrespective of renal denervation and SMTC. The metabolic data demonstrated that renal denervation lowered sodium balance during the first days after denervation (P Ͻ 0.001). These data show that renal denervation decreases MABP and renin secretion. However, neither renal denervation nor nNOS inhibition affects either the renin downregulation or the natriuretic response to acute sodium loading. Acute sodium-driven renin regulation seems independent of RSNA and nNOS under the present conditions. plasma renin concentration; total body sodium; blood pressure; sodium excretion THE INTERRELATIONSHIP BETWEEN blood pressure changes and acute variations in water and sodium excretion is not well defined. Arterial blood pressure is controlled by multiple systems, which differ widely in their time of activation. Neural systems react within seconds, while the hormonal and paracrine systems are more sluggish, requiring minutes to hours, or even days, to respond with full capacity. Neurogenic factors have long been hypothesized to be important in the initiation and maintenance of high blood pressure. There is considerable evidence suggesting that enhanced sympathetic drive to the heart and peripheral circulation is involved in the development of persistent blood pressure elevation or maintains the blood pressure elevation originally induced by nonneurogenic mechanisms (11). Moreover, it is known that electrical stimulation of the renal ...

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Section: Discussionsupporting

confidence: 66%

Renal nerves and nNOS: roles in natriuresis of acute isovolumetric sodium loading in conscious rats

Kompanowska-Jezierska

Wolff²,

Kuczeriszka³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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“…This may be due, in part, to the methods used to measure arterial pressure and how these measurements influence basal sympathetic activity. Such studies have included anesthetized surgically stressed animals (3), tail cuff measurements in conscious restrained rats (17), and direct recordings of arterial pressure in conscious tethered rats (21) or dogs (35). The strongest demonstration of how measurement conditions alter the influence of renal nerves on renal function comes from studies in conscious rabbits, in which renal nerve activity and renal blood flow were measured simultaneously in one kidney and blood flow was measured in the contralateral denervated kidney.…”

Section: Effect Of Bilateral Renal Denervation On Long-term Basal Levmentioning

confidence: 99%

Renal denervation chronically lowers arterial pressure independent of dietary sodium intake in normal rats

Jacob

Ariza

Osborn

2003

American Journal of Physiology-Heart and Circulatory Physiology

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.-The present study was designed to test the hypothesis that renal nerves chronically modulate arterial pressure (AP) under basal conditions and during changes in dietary salt intake. To test this hypothesis, continuous telemetric recording of AP in intact (sham) and renal denervated (RDNX) Sprague-Dawley rats was performed and the effect of increasing and decreasing dietary salt intake on AP was determined. In protocol 1, 24-h AP, sodium, and water balances were measured in RDNX (n ϭ 11) and sham (n ϭ 9) rats during 5 days of normal (0.4% NaCl) and 10 days of high (4.0% NaCl) salt intake, followed by a 3-day recovery period (0.4% NaCl). Protocol 2 was similar with the exception that salt intake was decreased to 0.04% NaCl for 10 days after the 5-day period of normal salt (0.04% NaCl) intake (RDNX; n ϭ 6, sham; n ϭ 5). In protocol 1, AP was lower in RDNX (91 Ϯ 1 mmHg) compared with sham (101 Ϯ 2 mmHg) rats during the 5-day 0.4% NaCl control period. During the 10 days of high salt intake, AP increased Ͻ5 mmHg in both groups so that the difference between sham and RDNX rats remained constant. In protocol 2, AP was also lower in RDNX (93 Ϯ 2 mmHg) compared with sham (105 Ϯ 4 mmHg) rats during the 5-day 0.4% NaCl control period, and AP did not change in response to 10 days of a low-salt diet in either group. Overall, there were no between-group differences in sodium or water balance in either protocol. We conclude that renal nerves support basal levels of AP, irrespective of dietary sodium intake in normal rats. sympathetic nervous system; angiotensin II; renal vascular resistance THE KIDNEYS PLAY A PROMINENT role in fluid and electrolyte regulation and therefore arterial pressure homeostasis. One mechanism by which the kidneys are thought to maintain fluid homeostasis is by the renal sympathetic nerves. Fluctuations in the degree of renal sympathetic nerve activity (RSNA) modulate renin secretion from juxtaglomerular cells, sodium reabsorption from renal tubular cells, and renal hemodynamics (13).Many lines of evidence have implicated sympathetically mediated mechanisms in the development of hypertension in several rat models (23,26,27,46). Accordingly, in some models of hypertension, complete renal denervation delayed the development of hypertension (23, 27-30). These results indirectly support a role of afferent and efferent renal nerves in the pathogenesis of hypertension. However, evidence suggesting that renal nerves are important in the long-term control of blood pressure in normotensive rats is not well established. For example, under conditions of increases in dietary sodium intake, is the reduction of RSNA important in the maintenance of a normotensive state? Although this is a crucial question, it has not been answered due to technical limitations for long-term recording of sympathetic nerve activity in conscious rats.The results of several studies (6, 33) tend to suggest that RSNA is modulated by changes in baroreceptor afferent nerve activity. The role of the baroreflex in regulating RSNA is in part sup...

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“…On the same day, the urinary bladder was split by a modification of our previously described technique. 16 Briefly, the bladder was accessed via a midline abdominal incision, and the urethra was tied. The bladder was divided approximately three fourths the length from the fundus toward the neck using a GIA 90 Premium surgical stapler (United States Surgical Corp, Norwalk, Conn).…”

Section: Surgical Proceduresmentioning

confidence: 99%

“…The catheters were exteriorized across the abdominal wall and connected to sterile plastic bags as previously described. 16 Approximately 1 week later, left and right retroperitoneal flank incisions were performed, and a silicone elastomer occluder was placed around each renal artery near its origin from the aorta. In addition, small-bore (nonobstructive) catheters were implanted into both renal arteries distal to the occluder to allow measurement of the renal perfusion pressure of each kidney.…”

Section: Surgical Proceduresmentioning

confidence: 99%

Role of pressure natriuresis in long-term control of renal electrolyte excretion.

et al. 1993

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If pressure natriuresis is to play an important role in arterial pressure control, renal perfusion pressure must have a long-term effect on urinary sodium excretion. The aim of this study was to quantitate the importance of renal perfusion pressure per se in controlling renal hemodynamics and electrolyte excretion chronically. Female mongrel dogs (n=6) were instrumented with bilateral renal artery catheters for measurement of renal perfusion pressure and occluders on both renal arteries for servo-control of renal perfusion pressure at different levels; the urinary bladder was split for determination of renal clearances and electrolyte excretion from each kidney separately. Because both kidneys were exposed to the same neurohumoral influences, any changes in renal function could be attributed to differences in renal perfusion pressure between the two kidneys. After 5 days of control, renal perfusion pressure to one kidney was reduced from 86.7 ±0.2 to 74.2 ±0.6 mm Hg for 12 days, and pressure in the contralateral kidney increased to 91.5±0.4 mm Hg. Sodium excretion decreased from 41±2 to 25±1 mmol/d in the servo-controlled kidney and increased from 41 ±1 to 55 ±1 mmol/d in the contralateral kidney during 12 days of servo-control. Urine volume, chloride excretion, and potassium excretion exhibited similar patterns during servo-control. In addition, autoregulation of effective renal plasma flow and glomerular filtration rate was relatively well maintained; however, in the low-pressure kidney, glomerular filtration rate was slightly but significantly lower (-8%) than in the contralateral kidney. In summary, long-term changes in renal perfusion pressure caused sustained alterations in renal electrolyte excretion. These results suggest that renal perfusion pressure is an important long-term controller of sodium and water excretion. over the long-term by complex interactions J~ A . between the various neurohumoral control systems and the ability of the kidneys to excrete salt and water. Guyton and colleagues 1 (see References 2 through 5 for review) have emphasized renal-body fluid feedback as the dominant control system for long-term blood pressure control. A key component of this feedback is the effect of arterial pressure on renal excretion of sodium, often referred to as pressure natriuresis. In most instances, this mechanism is believed to stabilize blood pressure in response to various perturbations that would tend to cause hypertension or hypotension.The validity of this concept depends on the assumption that arterial pressure has a long-term influence on renal excretion of sodium and water, a premise that has been difficult to test experimentally. Numerous investigators have demonstrated that acute changes in arterial pressure markedly alter sodium and water excretion, 69 but the long-term effects of pressure per se on renal excretion are largely unknown. Long-term pressurenatriuresis curves are usually determined indirectly by

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Role of renal nerves in compensatory adaptation to chronic reductions in sodium intake

Cited by 20 publications

References 0 publications

Renal nerves and nNOS: roles in natriuresis of acute isovolumetric sodium loading in conscious rats

Renal nerves and nNOS: roles in natriuresis of acute isovolumetric sodium loading in conscious rats

Renal denervation chronically lowers arterial pressure independent of dietary sodium intake in normal rats

Role of pressure natriuresis in long-term control of renal electrolyte excretion.

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